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- [00:02]
A
Welcome to season two of Derms on Drugs, a video podcast brought to you by Scholars in Medicine, the best educational platform of dermatology and provided at no cost to medical providers. Terms on Drugs is where cutting edge germ meets hit or miss comedy. I'm Matt Zyrus from Docs Dermatology and each week I'm joined by my residency buddies, Dr. Laura Ferris from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. And we use our 60 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be on the cutting edge of derm and you'll have some fun listening. New episodes drop every Friday on Scholars in Medicine, Apple Podcast, Spotify and other major podcast platforms. And just a reminder that there is a video component that has the key figures and tables from the articles we talk about. And this week we've got another one of our famous six pack episodes where we are going to go through the hottest, coolest stuff that we have seen in the literature. So I'm going to kick it over to Dr. Ferris to get us started.
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B
All right, so my first paper is safe and effective acne treatment across skin types with the 1726 nanometer CBUM Selective Laser 1 year data from a prospective multi center study.
- [01:11]
A
All right, Ferris, before you get into it too much, are you guys using this at the University of North Carolina? Do you guys have one? I don't think there are many of these in the whole city of Columbus.
- [01:23]
B
Like do.
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A
Is it, is it taken off or not?
- [01:26]
B
Okay, I think that I don't know how much it's taking off. It is not in a relatively poor state academic center taking off. Although I will say, like we actually do a lot of laser treatments. I know from training with you guys that none of us actually know a whole lot about lasers. Here's your opportunity to learn from people who don't know anything more than what's in the paper. But I thought it was really, I thought this was really kind of interesting.
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A
Yeah. Oh, this thing is fascinating. Sorry, go, go ahead, go ahead.
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B
Yeah, yeah, sure. What's the brand name of this thing? I just.
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A
Aviclear. Aviclear laser.
- [02:09]
B
Okay, so that's 1726 nanometers. What does it do? It basically like fries. So sebaceous glands. So it's like if sebaceous glands are at the heart of acne, can you just zap them and get rid of acne? Okay, so this was a study where they basically looked at one year outcomes and they had published their I think like 12 week outcomes previously. And you know, I know you guys will be like who cares if it works? You don't need one year data. But I actually think going to do a treatment for acne once and then stop it and you got to know if it still lasts. Right? Okay, so there we go. So sometimes I get some hate for doing one year follow up data studies. So no hate for.
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A
Yeah, because you're. We're trying.
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C
Right.
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A
The idea with this is to replace accutate and so we, you know, you want long term this. It makes sense. It makes sense. Okay, I'll allow it.
- [03:06]
B
So thank you. I thank you master. Okay, so this was an open label study. 16 to 60 year olds, Fitzpatrick 2 to 6. They had moderate to severe facial acne. So that's an IGA of three or four. There was like one mild who snuck in there but and they had to have at least 15 inflammatory lesions. So this is you know, kind of bad acne. And they had you know, across the spectrum. So and they were, they had three treatments with the Aviclear laser that were spaced two to five weeks apart. Now I was like well what else were they on? So they did have a 30 day washout from other acne treatments and then they could not be on any topical or systemic acne meds for the full year. And that was, you know, they did like fault. This doesn't let retrospective. It was prospective. So you know, I thought that's pretty rigorous because in reality like what I tell people, you cannot use tretinoin after this. No, I don't think I would. Okay, so. So this is sort of like the follow up. So between week 12 and week 52 basically there was no treatments. They were assessed. This was in Covid times. So they did like there were a lot of this assessments were done by, by photography. So they had standardized photographs and they had independent assessors but they were kind of blinded to like the study design and the time point. So so you know they may see like they weren't like here's the baseline, then here's week two. So they just were like here's some photos. Give your IGA score and give your lesion count. So kind of a decent way to blind. I thought if you look at the photo type of these patients, most of them were threes and fours. And if you look at their baseline acne, 77% were moderate, 22% were severe and 89 out of 104. So decent sized study completed. All of, you know, all of the visits, 71 were like PER. PER protocol. Meaning that they actually like had all their treatments and then followed up. So what did they actually find? Baseline mean inflammatory lesion count was 61, median 56. Like that's a lot of inflammatory lesions. And then at 12 weeks. Yeah, a lot of pimples. That's like bad. I mean, I call that bad acne.
- [05:29]
A
Yeah.
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B
And so, yes, on my IGA score.
- [05:32]
A
So these are people you would have put on Accutane, right?
- [05:35]
B
This is 100%. Yeah. The photos in there, I would have put these people on accutane. At week 12, their lesion count was reduced by 49.4%. And then at week 52, it was down to set. Was reduced by 70%. And so if you called a responder a reduction of 50% or more. At week 12, 79.8% were responders. At week 52, 91.5 in the per protocol. Like that was a little bit of a twist. Like the ones who actually did everything. 91.5% were responders. But even if you did an intent to treat analysis and you counted everybody with missing data as a failure, 67% were failures at week 52. So they kept getting better. Now, they also looked at non inflammatory lesions. They were down by 25% at week 12 and about 57% at week 52. IGA, by week 12, a third were clear or almost clear. And by week 52, 2/3 were clear or almost clear and Only like under 9.9% were moderate to severe. And there was like no difference in terms of subgroups of like this Fitzpatrick skin type, how their baseline severity, age, sex, safety, intolerability. It was like, you know, not surprisingly, everybody had erythema. Some people, most people had edema. There was some purging, which now we actually use as a medical term where like you get a little bit worse after you start. We see that with a lot of acne treatments. I thought 44%.
- [07:12]
A
I thought you meant.
- [07:13]
B
What's that? Not like.
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A
Yeah, they didn't develop bulimia as part of the treatment. Okay, yeah, okay.
- [07:21]
B
And you know, there was some of that, but it was generally mild. 18% had mild dryness. There was like some itchiness. No blistering, no hyper or hypopigmentation. The patient reported outcomes at baseline, 56% felt a lot or very much embarrassment or self consciousness about their acne. By 12 weeks, that went down to 14.6% by 52%, 8.4% felt very, are highly embarrassed. Whereas 90% said that they felt only a little or not at all embarrassed. So why does that matter? Because, you know, what acne really matters is like, how do the patients feel? Right. So all good stuff, pretty big. It was not a randomized control trial. There was not a control group. So that's not great. Everybody knew, every patient knew that they were getting it. But I think they did a. What they could to blind the readers. So, you know, how's this going to change clinical practice? Like, this is about 3,000, about a thousand dollars a session. So like $3,000 and it's out of pocket. You know, would I do this as somebody who could find $3,000 in my pocket if I had to? Would I do this for my kid? No, I would put my kid on Accutane. But people, some people don't want to spend, you know, like. So, you know, I get that there are people who want to avoid Accutane. I mean, interestingly, I'm in, you know, North Carolina in the Triangle area and like there's this huge case of a kid with acne who went out and like had a psychotic episode. Killed five people. I mean, it's terrible. This was several years ago and the defense was not Accutane, but Minocycline because it can cause psychiatric effects. So like there are going to be people who are afraid to treat their kids with drugs for ac, for acne. And I thought, oh, that's just Accutane. But now I think we're going to have the Minocycline. Not that there are other, aren't other things you can do. So interesting data. It's going to be expensive. And you know, just for fun, I was like, how is this, you know, relative to like Cab Trio, which we've done right that paper. So you know, the sort of the best, like apples to apples was that actually Cab trio at week 12 had like a 75% reduction in inflammatory lesions versus this was about a 50%. But cab trio didn't have like the one year data. If you look at it compared to Win Levy studies, there was like modest, you know, relative to vehicle. The inner. The inflammatory lesion was reduced by like 38% with wind levy at I think it was at 12 weeks versus 22% with vehicles. So you know, you would say at 12 weeks. This looks like it's better than Wind Levy. It looks like it is. You know, maybe not quite as immediate as Cab Trio, but it has long term data. So I guess there is some long Term data on out the six months with cab trio. But, you know, this is like three. Three shots and you're. Are three treatments and you're done.
- [10:44]
C
And.
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A
And it's. I'm sure these were worse patients than any of us would use for average.
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B
Win Levy. Yeah. If you look at Win Levy studies, those were like, mild to moderate, I don't think. Not moderate to severe.
- [10:56]
A
It.
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C
What I didn't see that the pro. I mean, they just. They zap your whole face. Like, what? They didn't really go into the protocol. And how big. Like, how long does this take? And does it hurt? I mean, have you guys had laser treatment? I've done PDL and laser hair removal. My word.
- [11:14]
A
Wait, that. That explain your hairline? Yeah, they were.
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C
They. That was the worst.
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A
They got him back. No, they got him backwards. They did PDL where he needed the hair removed and did the laser hair removal.
- [11:27]
C
Yeah, I'm like, why are you aiming it up there?
- [11:33]
B
You know, there was not as much of, like, pain as a side effect here. It was the edema and erythema.
- [11:40]
A
And I've known a few people. I've known a few people who've gotten it done, and it is in the same spectrum as, like, pdl. So, so painful. But people don't need, like, maybe topical numbing, but they don't, like, need it for sure. And it takes, depending on how fast the operator is, somewhere between 30 minutes and an hour to do a treatment.
- [12:06]
C
Okay.
- [12:07]
A
And so it. You know, the thing that I've been surprised is that we haven't seen more of using it for reducing oiliness and reduce. And sebaceous hyperplasia. Like those are, you know, if it reduces sebaceous hyperplasia and maybe reduces thickness of the skin. And people who, you know, have a lot of sebaceous stuff that I could see being, like, super useful just because we got nothing else if it's to address those cosmetic concerns.
- [12:39]
B
I think there. I think it does work in sebaceous hyperplasia. I vaguely recall, like, somebody talking to me about this once and that it does. I was like, gosh, could this work for hs? And I saw that they have some ongoing trials for hs, but.
- [12:54]
C
Right.
- [12:54]
B
So tylosabaceous unit.
- [12:57]
C
Interesting.
- [12:59]
B
You know, I'd be super interested in it if it worked for that, particularly with only three. I mean, you could say $3,000 versus the course of Accutane, but $3,000 versus Benzel for life.
- [13:12]
A
Yeah.
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B
See, Seems to start looking like a bargain. So.
- [13:16]
A
Yeah, that actually Makes a. A lot of sense. I had. That had never occurred to me at all.
- [13:22]
C
Okay.
- [13:22]
B
So kind of cool. Might make us want to learn about lasers all over again in our sunsets of our career.
- [13:29]
A
The other thing I remember about this, and the reason I think it's so painful because the, like, the key thing with this laser is that that wavelength is more absorbed by Sebum and Sebasty than it is by water. But it's like the absorption is like just barely above the water absorption. So you're still getting a lot of bulk heating because of the water in your skin heating up.
- [13:55]
B
You're boiling your skin.
- [13:56]
A
Yes, but it just. It's a little more heating up with the Sebum than it is of the. Of the general water.
- [14:02]
C
That's.
- [14:03]
A
That's the key thing about this laser.
- [14:06]
B
Yeah. And then I was like googling like, what's the nearest wavelength of another laser to 1726. And so the device that has other acne is the 1450 nanometer. Don't ask me what that one is. But that is also, like, there's some. There's some data on that. But the result, like, clinical results were apparently, like inconsistent.
- [14:30]
A
Okay.
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B
And one split face study showed no benefit over control. So it seems like there is something unique about really targeting, you know.
- [14:40]
C
Yeah.
- [14:40]
B
This the SIBA site. So kind of cool.
- [14:42]
A
Yeah. Makes sense. All right, Patton, what do you got?
- [14:45]
B
All right.
- [14:45]
C
My first six pack was published online January 2026. Clinical and experimental Dermatology, the journal of the British association of Dermatologists. In case anyone wondered, this article is titled Treatment with Mycophenolate Mofatil as an Adjuvant Therapy post Rituximab does not improve Treatment outcomes in Pemphigus. So kind of a spoiler alert in the headline there first. Author Vishvan Naidu. This was a letter to the editor. I like how they actually like letters to the editor. You actually say dear editor. Like it was just to them. It'd be funny if somebody was like, I can't believe you published that. That was just to you. There's never any form of closing, though. Like, I want to see a letter and then it ends with like, with deepest adoration. And then the author's name. Yeah, there's never. Yeah, there's never a sign off. It's kind of rude. All right, so some background.
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B
The editor has a name, for gosh sake. Be like, dear George, you know? Yes, I know.
- [15:41]
C
It's so.
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B
All right, we're gonna change this next time. I'm Gonna be like they're trying to make it.
- [15:46]
C
Yeah. Personal, but they don't make it personal like, either. Drop the deer all together. We're not kidding anyone. It's not like you're writing the guy a letter or just say, dear George. All right.
- [15:57]
B
Yeah. Okay. We're gonna, we're gonna practice.
- [16:00]
C
It's a movement. All right, so rituximab works well for pemphigus and pemphigoid for that matter, and is better than any other drug in allowing you to get patients to steroid free remission. The patient's relapse. Relapse rates vary depending on the source. I think 40 to 60. So I kind of tell patients like, yeah, 50% of patients like, it comes back. But, you know, we'll, we'll address it then. Kind of similar thing for bp. I mean, the rates really depend vary depending on the source you read. So is there maintenance therapy that should be given to prevent relapses? Right. This is the big question. Do you give maintenance ritux to everybody? When and how much do you do low dose pred. There was a study from Taiwan that suggested azathioprine could prevent remission. I'm sorry, prevent relapse. But I don't think that's a widespread practice. The authors of this study, practicing at King's College in London, say that they routinely prescribe either low dose mycophenolate, 500 to 1 gram, or aine azathioprine, 1 mig per kig after rituximab therapy to prevent relapse. Like, that's kind of their standard. But does it actually help prevent relapse? They investigated a retrospective review, compared 33 patients that got low dose prednisolone plus mycophenolate following rituximab treatment to 17 patients that got only low dose prednisone. So kind of a small study in the MMF patients plus prednisolone outnumbered the prednisolone patients kind of significantly. Length of follow up, 36 months. Figure 1b. No difference in percentages of patients with complete remission, partial remission, or no remission. So there wasn't any difference. Overall percentage of patients while they're still on the rituximab.
- [17:43]
A
Like, is it ongoing through the rituximab?
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C
I would say no. That. And, and I don't think that they specifically, like, when did we start this? My guess is they got the two doses and then they just started it right away.
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A
Okay.
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C
All right. All right. The percentage of patients in Complete remission was actually higher in the prednisone only group, but it wasn't statistically significant. Maybe the prednisolone only group relapsed earlier. No, that didn't happen either. Figure 1c shows similar durations of remission between the two groups. Were there any differences in anything that was measured between the two groups? There was. CD8T cell counts were lower in the group that received prednisolone plus mate, which led the authors to conclude, they're not going to do this anymore. They're not going to give mycophenolate mofatil as maintenance therapy because it doesn't seem to help with remission rates. And by decreasing the CD8T cell counts, the authors hypothesize that may predispose patients to infections. So they did a study, you know, that demonstrated their standard of care, so to speak, of maintenance. Mycophenolate may not be a good idea. It was kind of interesting.
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A
Do you use it or do you, Is it, is it, have, have you been using it? Are you going to stop using it? What's your.
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C
I don't do any, like, you know, the, the. So, I mean the, the mycophenolate's interesting because it's low dose and that would, patients are going to tolerate that and I doubt you're going to run into too many problems. Yeah, but the other question, is maintenance, like, maintenance therapy at all? Like, do we have any really, really good evidence that there's a certain maintenance therapy that everyone ought to be using? I don't do any maintenance. They get rituximab, a fair number of patients. You can taper off the corticosteroids and you know, the, the original rituximab protocol that was published in the Lancet, Those patients got 500 milligram, like a touch up dose, let's call it at month 12 and month 18. And then the Vicky worst study that was published in New England Journal of Medicine, I'm pretty sure she gave the two doses. And then at six months, patients got another two doses. So the studies so kind of supported, hey, yeah, we should do this. But I do not. I mean there's a fair number of
- [20:02]
A
patients where, yeah, if you don't need it and if you, yeah, you don't
- [20:05]
C
need it and it's not like, you know, maintenance Ruxolitinib with your atopic therm to keep it under control. Right. Safe and whatever. Rituximab, Zylican iv.
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A
Do you tell them so?
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C
No, I, I Do I don't do any maintenance therapy.
- [20:21]
A
Do you tell them like, okay, if you get one blister back, if you get one thing back, immediately let me know and let's get it moving because you know it's coming.
- [20:30]
C
Yeah, right. I mean, the mouth especially. Right. I mean, for whatever reason, skin clears really, really well. Mouth can be stubborn. So it's like you notice blood on your toothbrush, toothbrush, you call me, we'll see where your titers are. If the titers are elevated and they have the symptoms, pretty low threshold for getting him back to the infusion center. Okay. If the, if the titers are normal and they're like, I think I got a blister, but it's not documented. And then I. I kind of wait. Okay.
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B
Okay. And they, they didn't follow desmoglean1 and 3titters. But I didn't see. But I probably didn't read it carefully enough.
- [21:12]
C
No, they didn't follow titers. I'm pulling it up. I'm pretty sure they did not. Would you.
- [21:16]
B
Do you.
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C
It was. It was a very, very short. I mean, it was truly a letter.
- [21:20]
B
It was a letter. That's right. The editor has a very short attention.
- [21:25]
C
He's the worst.
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A
Should have to calligraphy.
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C
And he never writes back. It's so rude.
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A
All right, we're moving on to. To mine here. So first, first one was a hot topic. So, you know, does dupilumab increase the risk of cutaneous T cell lymphoma in patients that get treated with it? Title of the article was dupilumab treatment is not associated with changes in lymphoma risk and atopic dermatit type 2 inflammatory diseases. Data from a large scale retrospective cohort study. It was in Frontiers in Medicine. So this is basically a trinetic study. They looked at a whole bunch of people who got atopic dermatitis. It got dupilumab or got some other drug. And then they also looked at people who had other type 2 diseases. And the basic takeaway first that whether you get dupilumab or not, you've got a. If you are diagnosed with atopic dermatitis, your probability of being subsequently diagnosed later with with CTCL is 10 times higher than the background population. The actual number, and this is now across multiple studies I've seen, this is about 1 in 600 people who are diagnosed with AD will eventually be diagnosed with CTCL. Unknown if it is that it was CTCL the whole time and it just looked like AD on, you know, pathology and Clinical or if it was AD that truly turned into ctcl. We truly don't know the answer to that. But we do know 1 in 600 people who are diagnosed with atopic dermatitis are later diagnosed with ctcl. That is not a. There's not an elevated risk in people with other type 2 inflammatory diseases. Uh, and then so people with AD, you know, had a with compared to people with other type 2 inflammatory diseases, had a similarly increased risk in the risk of. In the likelihood of non Hodgkin's lymphoma, had a similar. But. But then also had elevated risk in T cell and natural killer cell lymphomas, and had a pretty dramatic increase in the risk of eventually getting Cesare. So it really is like AD predisposes to a later diagnosis of ctcl. So then the question is, what about dupilumab versus other systemic treatments? Absolutely no increase in the risk of Cesare. I'm sorry, in the risk of ctcl. The non Hodgkin's lymphoma, though dupilumab dramatically reduced the risk, so hazard ratio of 0.44 compared to people treated with other systemic therap. And it also dramatically reduced the risk of Cesare, so reduced the risk of Cesare by 92%. So a hazard ratio of 0.08. But CTCL risked no effect. So it really does look like DUPY just might reveal ctcl, but it does not. If it does, it does not promote progression at all. But.
- [24:41]
C
So the.
- [24:42]
A
This trinetic studies. You know, I'm always a little nervous with trinetic studies, but this, this was well done and these were high powered offer high powered authors. So I. This goes with what I thought anyways. And again, it reconfirms that DUPY reduces your risk of. Of hematologic malignancies overall and dramatically reduces your risk of Cesare syndrome. So.
- [25:08]
B
Okay, I have a question. Yes, you people often say prigo nodularis and atopic dermatitis is the same thing.
- [25:16]
A
So patent tends to.
- [25:18]
C
When I, When I see a pure. A pure prurigo nodularis patient. When I, When I see prurigo nodularis patient, and this was before doopie even came out. Like my, my pure agonodularis patients, I'm like, okay, atopic term. I'm dealing with an atopic term patient and we're going to manage it like this. I mean, and when I still CPN patients, like, I just get that feel from them. Like it just like it smells like a topic.
- [25:53]
A
So Patton's doing vibe dermatology yeah, like, yeah, man, the 80 virgin. So there is, there is some data where they've done biopsy studies of, you know, AD people with ad, people with PN and people who have both and they're, they're similar, but they are distinguishable. But it's, it, it really comes down to this question of like, where do you draw the line of they're similar but not identical? Like, it's a, it's a reasonable question. My, my belief is that there, there are people who have both and there probably are people who have just the neuro hypersensitivity and the rest of their skin is totally fine, but functionally I don't care.
- [26:41]
C
Right.
- [26:42]
B
Again, this, I want to cut to the chase. Is this like shouldn't do PN patients get CTCL more? I've never seen that reported.
- [26:51]
A
Not to my knowledge. I don't know if anybody's ever looked at.
- [26:55]
C
They do. I'm making that up. I'm sticking with my gun, so why not?
- [26:59]
A
It's a vibe. It's vibe data. Fanatic vibe data. All right, here's my other one. So this one is, is me announcing to the world that I was very wrong about something. So I. Wow. Yeah. Yeah. I, When I'm wrong, I take, I, you know, so I have numerous times said, hey, it's in the label for doopie that it may increase your risk of parasitic and helminth infections, but there's absolutely no data of any unusual or unexpected parasitic or helminthic infection. So that was theoretical, not real. I was wrong. Scabies. Doopie makes scabies worse.
- [27:38]
C
I don't, I don't know that you were wrong, but. Okay, go on.
- [27:41]
A
Well, but it's a parasitic infection and doopie, it makes it progress to be like Norwegian scabies. So people get crusted scabies probably because TH2 immunity is playing a role in biting the parasite off and it may be hard to identify. So there were a few, several reports of this in the literature. But it may like reduce the itch significantly. Not in all of them, but in some of them. But then people get like morphology of crusted scabies. And when I brought this up, like my, my one of my partners was like, oh yeah, that happened to my dad. Like he had, my father in law, he had cancer and started to get itchy. We thought it was one of the checkpoint reaction inhibitors put him on doopie. Then his rash started to look weird and son of a gun, it turned out he had scabies.
- [28:35]
B
But do you think that he, that the doopie made him susceptible to scabies or did he get, did he get doopie because he had scabies?
- [28:43]
C
Untreated scabies.
- [28:44]
B
Right.
- [28:44]
C
I mean, these, these patients have. Untreated.
- [28:47]
B
I've seen this happen before, but they get somebody that's babies and they get put on duty and, and.
- [28:52]
A
But the thing that was interesting here, that it turned into Norwegian scabies in normal people.
- [28:57]
B
Yes, because I, I could see that. Why do people get Norwegian or now what we call crusted. Just because the Norwegians are beating us in the Winter Olympics doesn't mean we need to name is scabies after.
- [29:08]
C
No, we're, we're, we're bringing that back.
- [29:10]
B
We're going to bring it back, damn it. You got the gold medal. But you also have the worst scabies, worst babies.
- [29:18]
A
So that should become part of Trump's foreign policy that, you know, we're going to name a bad disease after your country. Exactly.
- [29:28]
B
No, but I, I digress. Where was I going with this? I. But I do think that crusted scabies comes, you know, I mean, we've gone through this whole thing. Scratching is protect against parasites. If you're not itchy, you don't scratch. Say the parasites are going to multiply. So I could see it. Now, I will tell you my personal. It's not personal. My experience is I have had a couple patients who I put on DUPY who have gotten rip roaring. Demodex.
- [29:57]
A
Yeah, yeah, I've seen that a couple of times.
- [29:59]
B
Right. So that's to me, the parasite thing.
- [30:02]
A
Yeah. And, and it, yeah, that's an interesting. I think Demodex and scabies both. And it really goes back to me to the idea that if you put somebody on doopie or any of these AD drugs and they don't like, get dramatically better pretty quickly and stay dramatically better, you shouldn't just be like, well, it's still A.D. let's try another drug. That's probably what's going on. But you should really, like, if the first drug doesn't work great, you should really think about patch testing, think about biopsying. That's in. You have to do any of that. But you should really think about that. Especially if, you know, if they get 50% better, looks the same, they just didn't get better enough. That's different. They didn't really get any better or changed or got worse. That's somebody that you really got to be like, what the hell is going on here?
- [30:49]
C
The most recent scabies Case that I saw that that was it, he was on doopie and it's kind of like, yeah, that's kind of weird. Like you're not any better whatsoever. Yeah. And he had scabies. Yeah.
- [31:01]
A
And that's actually reminds me the other thing for our listeners, if you haven't seen this before, the new thing in scabies is that woods lighting them works. So scabies mites fluoresce as like a little yellow dot and then the burrow behind them fluoresces is like a white. Looks like a little smokestack, a little smoke coming off of the scabies mite. So that's, to me, that is now the most sensitive way to diagnose scabies. If it crosses your mind.
- [31:31]
C
And I have an AI answer. Larson et al. 2018, cross sectional analysis of 695 PN patients from the Johns Hopkins Health System compared to 2.4 match con, 2.4 million match controls for primary cutaneous lymphoma, which was predominantly CTCL. The odds ratio was 24.8. What?
- [31:55]
A
You're making that up, Patton.
- [31:57]
C
I mean, AI may be making it up, but I am just reading what AI told me. AI knows it has to make me feel good. So this could all, all be made up like. Yeah, Dr. Patton, you were right.
- [32:10]
A
True. You know, and by the way, I'm coining a new phrase from now on that there's AI and bi. Right. Artificial intelligence and biologic intelligence. Right. So that's we are just entities that have developed bgi, biologic general intelligence. And now the machines are catching up with us. Artificial general intelligence. There we go. All right, let's move on. Ferris, what do you got?
- [32:34]
B
Okay, I have from the JAD, hyperkalemia incidence in females over 45 years old on spironolactone for dermatologic conditions, a retrospective cohort study. And this was by Gregoire et al. This is Arashimo Staghini and John Barbieri, who were the senior authors on this. Okay, so spironolactone in, you know, your coolest acne patients, women over 45. And so we do know that, you know, we've had that this group has done a lot to say like, you know, we can, we can pull back on monitoring for a lot of things. Like, you know, we can thank them for not having to check labs on accurate, for giving us the confidence not to check labs on accutane. And then they've looked at spironolactone, but the word has always been like fine for women under 45, but over 45, there's some risk of hyperkalemia. So the key question was, you know, for women 45 and older, how often do we see hyperkalemia? Who's at risk and what should we do about monitoring? And they also looked at, like, what do people actually do? So this was a time, 10 year timeframe, 2015 to 2020, 25. They looked across indications. So it's basically acne, female pattern, hair loss, hirsutism and HS. And they had to have at least two prescriptions. And they narrowed this down to about 398 analyzable patients. They also looked at comorbidities like hypertension, diabetes, chronic kidney disease. And then if they were on, like, what they called risk compounding medications. So ACE inhibitors, ARBs, beta blockers, diuretics, and they, they looked at potassium labs at three points.
- [34:26]
A
So wait, I gotta. Wait, I gotta jump in for one second. There's one other, one of our listeners, actually, after we talked recently about Bactrim killing people who have, who get it for acne, especially young, healthy people, one of our listeners emailed me that and that it Bactrim also causes hyperkalemia. And so if you have somebody on spironolactone and they get Bactrim, it can cause them to get like severe hyperkalemia that can even be fatal. Actually was from Dr. Dennis Newton at the University of Texas Southwestern.
- [35:07]
B
Oh, good. Okay.
- [35:08]
A
I did not know that Bactrim.
- [35:10]
B
No, I did not either. And that is not an inconceivable thing that could happen. So.
- [35:15]
A
Yep.
- [35:16]
B
Okay. So they defined hyperkalemia as a potassium 5 or higher because their lab upper limit of normal is 5. Like, so I mean, 5.1. Do I lose sleep over that? No, but that would be in their, you know, in their outcome hyperkalemia. And then so mean age was 54. These 62% of them had no predisposing comorbidity and 70% were on no risk compounding meds. Most of these were acne, 47.5%, not most. But the highest use was for acne and then hair loss at 37%. Most common starting dose, 50 milligrams, max dose. Most common max dose was 100 milligrams a day. So, you know, and then 61% had at least one dose increase. So monitoring was like all over the place. So if you look at. Because, you know, we say, like, oh, we should do this. 70% of patients had a potassium within a year of starting post initiation, within six months was 58.5%. And really, if you look at it, it's like the guy, the package insert actually says that you should have, like, potassium checked within a week. I don't think I ever knew that. So 19. Only 19% had it within one week, and only 30% had it within four, four weeks. 58% had potassium checked within six months or of reaching their maximum dose. So, like, in the real world, do we follow the label? We don't really. Okay. Incidence of hyperkalemia, 10%. And among those with those baseline and interval labs, 13% developed hyperkalemia after starting spironolactone. They were mostly mild. 97.5% of these had a potassium of 5.1 to 6. The mean hyperkalemic potassium was 5.3. There's one patient who had a potassium over 6. When did it occur? On average, at 20.5 months after starting spironolactone. So it's not this like, oh, this happens within a month. There were only three cases, in fact, when it occurred within one to four weeks of initiation, which is like the window where we're supposed to be worried about it. Most common dose associated with it, 100 milligrams. There was no significant relationship between dose and degree of elevation. So who were the people most likely to have it? It was patients over 60, 65 or older, those who had one or more comorbidity and the dose was not associated. And, you know, again, like, if you combined all these things, like you were over 65 and you had hypertension, you know, your risk went higher and higher. Most of the time, hyperkalemia was 85% of the time asymptomatic when it was present. That, like, the symptomatic was like fatigue or gi. There were like, the only serious event they had was one episode of brady cardia with qt. QT changes. But they actually attributed to the beta blocker and their calcium channel blocker and not to the spironolactone. And most of them were like managed outpatient. And that patient was not even start. It wasn't stopped. So 62% of cases, nothing about nothing changed. They did not drop the dose, hold it. There were dose reductions and temporary holds, like 12 to 17% of the time. Only 3.8% of the time did they actually, like, change their care, meaning that they, you know, that they did something different. So basically, most patients did not have a management change.
- [39:16]
A
So what's the summary? Was their recommendation a cause?
- [39:20]
B
It.
- [39:20]
A
It sounds to me like this, you know, as you know, faris, when you do trials and you're just checking labs, like on a monthly basis and everybody, you pick stuff up. So, you know, without a comparison group, it wouldn't shock me if you saw this much hyperkalemia in a normal group of like. So do they recommend. Do they give any clip? Like, we should do it. We shouldn't do it. Like, did they say anything?
- [39:44]
B
No, I mean, they. There wasn't like a strong recommendation. Like, they said, still, you know, if you have women 45 to 64, you know, if they're on like renin angiotensin. Renin angiotensin, aldosterone system, medicines, monitor them, you know, maybe at baseline and one to four, you know, months after. For women who are over 65, especially if they have comorbidities, we should be probably following those women, like, who's a
- [40:14]
A
65 year old who's still on Spironolactone for.
- [40:17]
B
I know, I was thinking about that. Like, I have not had.
- [40:21]
A
Right.
- [40:21]
B
You know, I can't imagine. I can't remember the last time I used spironolactone on somebody over 65. Yeah. So like, basically it was like 45 to 65, you're healthy. Maybe do like a baseline one check and then just follow them. And if you have comorbidities and 65, then you can do some checking. Probably it's baseline in that first month and then maybe periodically. Probably that age group, to be honest, is getting BMPs and CMPs kind of for other reasons. So I think we don't worry a lot about this. But yes, they did acknowledge, because there wasn't a control group here, like, how much of this was hemolysis in the labs or, you know, rechecking, and then it came down to normal. So I don't think we got a lot of super helpful answers out of it other than it still, even in the higher risk older women group, it still wasn't a big deal.
- [41:19]
C
Yeah, I've had older women who want to do everything for hair loss, female powder and hair loss.
- [41:26]
A
Oh, yeah, yeah, yeah, yeah.
- [41:27]
C
And so they're like, I'm gonna. And I just had a patient, like two weeks ago, she came in, she's like, my PCP is making me stop the spirona. I'm like, okay, Yeah, all right, it's a good idea. You should listen to him.
- [41:46]
A
Right, Pat? But. All right, Pat, what do you got?
- [41:49]
C
All right, my second six pack, I'm doing. I'm doing a third. You guys are doing thirds. I have a really quick. It's like a blurb.
- [41:56]
A
Okay, so it was that. You're slowing it down.
- [41:58]
B
Just go to the chase.
- [41:59]
C
Assessing disease progression in Hurley 1 Hydride 90 Supper Tiva patients. A nested case control study by Rodriguez Santa et al. It was available online in the journal Dermatology February 2026. Retrospective study 2 aims. Aim 1 follow Hurley stage 1 patients determine the incidence of stage 2 and 3 disease. Aim 2 performing nested case control study of stage 1 to identify what factors, if any, were associated with progression. The study was performed at the Virgin de las Nelas. I'm probably butchering that. University hospital in Spain from 2017, 2024, 133 Hurley Stage 1 patients. This was based on clinical and ultrasound. All patients got ultrasound exams every, like, visit. Average follow up was just under two years. The answer to the big question, how many patients with stage one disease at baseline progressed to Hurley stage two or three? It was 50 out of the 133. So 37.7% of stage one patients progress. A Kaplan Meier curve shows that the median time to progression was 308 days. So of the patients who progress, about half will do so within the first month. I'm sorry, the first ten months, only one patient progressed to stage three. Everyone else progressed to stage two. There's three tables with lots of numbers. Table one and two show baseline and follow up characteristics. Table three, kind of interesting, compares the patients that progressed to the patients that didn't progress. And according to multivariate analysis, the factors that were associated with progression were the number of cigarettes smoked per day. So progressors smoked more cigarettes on average compared to non progressors. If you were early stage 1C at baseline, you were more likely to progress. I mean, 80% of the patients were like, stage 1A, stage 1C.
- [43:50]
A
Like, I didn't even know. There was like, what's this ABC stuff?
- [43:54]
C
Yeah, there was like a paper from a Dutch group or maybe Danish group, and they're like, let's break down stage one A, B and C. And one is like a few lesions but without tunneling. And three is like lots, and then two is just kind of somewhere in between. It wasn't. I mean, it's kind of a. Honestly, I think the reason they did it was because these drugs are approved for moderate and severe disease. And if you have stage one, they're like, if we call it stage one B, we can call that moderate and stage one C severe, which I think is actually like, true.
- [44:30]
A
I would agree, but. And you know, if that Study came out of Denmark. We should now call it Danish hidradenitis.
- [44:36]
C
Yes.
- [44:37]
A
Unless they give us green. Unless they give us Greenland, then. That's right. We'll let them off.
- [44:42]
C
That's right. So an increase in the number of abscesses, but not inflammatory nodules, was associated with progression. And finally, patients that had more punch drainages performed were less likely to progress, suggesting that this intervention, punch drainages may help prevent progression to early stage two or three. I mean, that's, you know, reading into it a lot. So focusing on some of these things. The authors say that encouraging patients to smoke fewer cigarettes may be a kindler, gentler way of broaching the smoking issue. Because we're all supposed to be like, fluffy, happy, agreeable doctors instead of, you know, meaning people.
- [45:19]
B
They're like, we're not saying you can't smoke any cigarettes.
- [45:22]
C
That's right. Just smoke viewer on them. Which actually, I could see patients being like, okay, yeah, yeah, I'll try. Instead of being like, quit smoking.
- [45:30]
B
Right. Apparently, that's still too many.
- [45:33]
C
It maybe was a little interesting. BMI didn't differentiate progressors from non progressors. So it's not like the non progressors had statistically significant lower bmi. So the other area where we're all supposed to be touchy feely didn't really seem to matter. And then, you know, I guess drain the abscesses. Right. Kind of important. It takes time. Maybe in a busy clinic, it's tempting to be like, just take some doxy and hopefully those will go away. Maybe the drainage does prevent tunneling. I mean, you could buy it, right? You leave an abscess there and theoretically could tunnel. And I also think HS patients can be procedure averse, understandably so, because, like, a traumatic ER experience. And am I implying that ER practitioners don't know what they're doing? Yes. Yes, I am. When it comes to dirt, maybe discussing this paper, like, in encourages patients like, look, there was a study. It showed this could actually be helpful. Everybody, maybe that's a little strong, but maybe this will help prevent, like, a tunnel to form. So, yeah, that's all I got. What they. What they didn't. They looked at, you know, progressives versus non progressors. What percentage of them were given antibiotics? And it was about the same between the two groups. They did not do the same analysis for biologics, which I thought was.
- [46:52]
B
I didn't know if maybe there weren't enough patients in there or maybe it's hard to get biologics approved for early stage one.
- [46:59]
A
So it Wasn't indicated.
- [47:01]
C
It was weird that they did it for antibiotics. And. And they did that analysis for antibiotics. Like percentages prescribe this. Yes. No progressors versus non progressors. And they didn't do it. They didn't ask that same question for any other drug.
- [47:14]
B
That is the question we need is do biologics prevent. And then like topical ruitinib, which now has some data. Right. Like, that's what we really need to know is can you prevent progression?
- [47:26]
A
But wouldn't. Wouldn't it have just been that they. If. If you're Hurley1 you're probably not. They won't give you a biologic.
- [47:35]
C
Yeah, but they. They had median duration of time on biologics. So the patient's got biologics. Maybe, like far said, maybe it was such a low number that they didn't.
- [47:49]
A
Okay. All right. All right. What's number two?
- [47:53]
C
Case report. Zinc deficiency is a modifier modifiable risk factor for enfort nab vedotin induced cutaneous adverse events. So this was in frontiers of oncology, November 2025. 10 patients treated with EV that developed either dysgeusia skin rash. 4 patients got zinc, and 3 of the 4 had the SD rifle. SD rife like rash resolved. They were all low in zinc. And so I just. This article popped across my. Whatever. And then we just had a patient with this rash. And I'm like, check a zinc. And it was low.
- [48:27]
B
So she gave him zinc. We did see if they get better. And it was interesting. I saw that paper that the discusia did not improve with. The sanctum.
- [48:37]
C
Did not improve. Dryness got a little bit better, but it didn't resolve.
- [48:41]
B
Skin got better.
- [48:42]
C
From the previous article of preventative topical clobazol in the. The susceptible areas. That really seemed to work because that was a split study. It was kind of impressive. Yeah. So you give all these patients zinc, and you slather them with clobazol.
- [48:56]
A
You know what would work great? You remember that old zinc cap? The. It was the foam that was supposed to be just a zinc peritheone foam, but it actually had clobatazole in it.
- [49:08]
C
Yeah, I do remember that.
- [49:09]
B
Yeah.
- [49:10]
A
Because it was. It was like.
- [49:12]
C
I did a. I did three papers. I'm cool, like you guys.
- [49:16]
A
All right. That's good. That's good stuff. All right. All right. My last two number one Jack inhibitors and memory impairment. A disproportionality analysis in the WHO World Health Organization global pharmacovigilance database called Vigibase. So generally, I do not believe anything in these databases because as soon as you say, hey, you might get a side effect of xyz, then when people get X, Y or Z, whether it's related to the drug or not, they report it. So then it looks like there's more cases reported with that drug. This one matters a lot to me because nobody's telling people with a JAK inhibitor, hey, you might get memory impairment. So this is exactly how these are supposed to be used. And son of a. This, like, it was. It was significant. So, like, the, the risk of getting memory impairment, I was greatest with Tofacitinib. The majority of these people were getting them for rheumatoid arthritis. But like, Tofacitinib had a. An odds ratio or reporting ratio of like three, so. And it was significant. These were most of. Over half of the cases were non elderly patients, and a third of them were like, serious memory impairment, like, like meaningful cognitive impairment. The. There's not enough data in vigibase to like, really describe, like, does it go away whenever you stop the drug? But in the case that these people had, that triggered them to look at this. They stopped it, and it did go away. And mechanistically, it does make some sense because there are these neuroprotective agents that activate the JAK STAT pathway. And so whenever you block them, you may, like, not have these neuroprotective effects. So it was. It's like a really interesting new thing that, like, I think we probably need to start telling patients, like, hey, if you notice your memory, like, seems off. But I. I still don't know if I'll tell people. It'll more be like if they bring it up, like, hey, bring it up.
- [51:26]
B
Then we'll be like, huh, that's interesting.
- [51:29]
A
Yeah.
- [51:29]
C
But I remember this was reported.
- [51:31]
B
I told you that when you started this.
- [51:34]
C
Don't you remember it?
- [51:35]
B
So, yeah,
- [51:41]
A
But this.
- [51:42]
C
This came up. I remember this with like, statin. Remember that was a thing with statins at one time, and it was like, oh, this. And then, you know, right now they. They have done multiple prospective randomized control. Like, the statin thing didn't seem to be something that happened. They still say, you know what? Rarely. Yeah. That we don't know what that is. And so maybe it's the same thing with the Jack. It would have been interesting. The case that they present is pretty impressive. And it was one patient, but they said six weeks. The issue she was having completely resolved.
- [52:14]
A
Yeah.
- [52:15]
C
So they should have put it back
- [52:16]
A
on it and retested and it took a long time. People were generally on the drug for, like, I think, like, a year before this started. So it did seem to be, like, kind of a cumulative toxic effect. Yeah, it's interesting. Like, new, unexpected. It's the kind of thing where you're like, well, with the new drug, you never really know. Well, son of a bitch. We didn't. Like, maybe this. Maybe it is a thing, maybe it's not a thing. But I'm sure a lot more stuff will come out now then my last one. This was just a great. Oh, love it when this kind of stuff comes out. So development of a patient decision aid for atopic dermatitis, systemic treatments in adults. And so it's just a great example of how dumb physicians can be. So these were, I think, a bunch of academic physicians and then a bunch of patients, and they wanted to come up with a patient decision aid where, like, the patient. You give it to the patient. It helps them, like, understand the different drug options and whatever. So the doctors made it. The patients were like, way too complicated. Can't understand it at all. Went back to the doctors, they made it more complicated. The patient said, no, this is terrible. Like, we can't. And then they went back to the doctors, like, nope, we need to add more. There are not enough of the risks discussed. So they added. It was like they just kept getting further and further away of the patients being like, please, we can't understand this. And the doctors being like, well, we need to give you more information. Like, just the main takeaway. Now, there was one useful thing here, and it was this, that the best way to approach shared decision making with a patient is with staged decisions. And, like, that's what got me excited about this. That's what I've been doing forever and trying to tell people to do. Like, you give patients one question at a time. Like, I always give them an A versus B. Do you want this? And so for me, it's, do you want a pill that'll weaken your immune system or you want a shot that won't? Okay, now if you say very unbiased question.
- [54:16]
C
Well, but it's true.
- [54:17]
A
It's true.
- [54:18]
C
It's true.
- [54:19]
A
It's accurate.
- [54:20]
B
Right.
- [54:20]
A
And then if they say we don't
- [54:22]
C
get paid by Regeneron at all.
- [54:24]
A
Yes. Right, right. Yeah.
- [54:26]
B
There's no.
- [54:26]
A
I mean, I do, but not for this.
- [54:28]
C
Yeah.
- [54:28]
B
You get paid. Yeah. More than anybody I know.
- [54:31]
C
Right.
- [54:31]
A
And then if they say, I want a shot, then I'm like, okay, this shot is once every two weeks, forever. But if you got allergies or asthma, it'll help. We got other shots that you don't have to take as frequently, but they don't help with allergies or asthma. Okay. And then they. Okay. And then if there's. Well, I want the one I don't have to take as much. Okay. This one might cause bloodshot eyes. The other one doesn't cause bloodshot eyes. Which one do you want to do? Like, it's, it's so it's like A versus B. You always give people this or that. Not like, okay, you've got five options. We could do JAK inhibitors. We've got two of those. We could do, you know, dupilumab. We could do trilate. Like, here's the. No, people cannot understand that. You give them one thing at a time. The other thing that, that always reminds me is, is how. And I'd be interested what you two do. I'll say what I do first. So when the patient's like, what would you do? Right? Because some people like, well, I always tell the patient that what I would do is irrelevant to what they should do and the blah, blah, blah. I always tell them, look, I'm going to tell you exactly what I would do. But just remember, this is like being at a restaurant. Like, if we were out at a restaurant, I'd been there before and you hadn't, I might be like, oh, this. I would get the salmon here and you could be like, I hate fish. Like, so, like, yes, the salmon's good here, but it's not what's best for you. Same thing with the drug. And then I say, okay, so here's what I would do. But I'm not saying that's what you should do. How do you guys handle it? Whenever a patient says, what would you do?
- [55:59]
B
I tell them what I would do. Okay, Patton, it comes up with like, at like kids, like, what would you do? Accutane, Biologic, whatever. I mean, not like, I don't really see kids, but it's like, you know, with like 18 or 20 year olds, parents will ask that. Or like, you know, yeah, people ask that. I will tell them what I would do.
- [56:19]
A
Patton, what do you do?
- [56:22]
C
Kids with Accutane, that helps? Like, hey, my kid had this. This is what I did. And then I think they're like, okay, yeah, then that. That's what I want to do, man.
- [56:32]
A
I don't know.
- [56:33]
C
I mean, in the instance of atopic derm, to be honest, I'm like, the, the. The shots are safer. There's one that was FDA approved before any of them. And like, total conflict. Like, I do. Regeneron does pay me for, like, BP stuff, but so, but that. So you should know that. But I'm like, the shots just like the safety profile. You don't have to get blood work. You know, I don't care if your kidneys fail. You're like, it's just in so many patients are better and so many patients stay on it because it changes their life. And I strongly, strongly recommend that. Are you good with that or do you want to hear about other things? That's how I start off my ad. Like, and granted, like, yeah, I'm pushing them towards dupy, but I think there's good reason to do that.
- [57:22]
B
Yeah, there's just. There's the most patient years of exposure to say, like, here are the risks that we know. And, you know, I think, you know, when I read the package insert of JAK inhibitors for atopic dermatitis, it pretty clearly to me says, you should start with a biologic.
- [57:41]
C
That's.
- [57:42]
A
And that is a reasonable. It's. It's hard for me to. Unless somebody says, like, I really can't see giving myself, like, I. Needle phobia is the primary thing that, like, I'll use jack first line. If somebody's like, I. I can't give myself a shot. I don't want to give myself a shot. I don't want anybody else giving me a shot. I don't want a shot. I'll use a jack first line there. But I. I agree. I mean, it's, you know, they are immunosuppressive. Whether they have other side effects or not, I'm not. I don't know. But they're definitely immunosuppressive. And the shots are not.
- [58:14]
C
You know what I have come to appreciate, like, within the last three months that I never really thought about before.
- [58:19]
A
Wait, I bet I do know beauty.
- [58:23]
C
No, I've always appreciated beauty.
- [58:24]
A
Okay.
- [58:25]
C
That's a weird thing, is that dupilumab hurts. Like, I have talked to people that are like, yeah, I have given myself shots of other things. Doopie is very, very painful.
- [58:40]
A
Yeah. And compared to the other drugs, very true. I think doopie and then the. I. I think Libry's less painful. Trelo, I'm not sure. And Nemo just doesn't hurt at all.
- [58:52]
C
So that is my one, like, downsell with doopie is like, you know, here's what's been around longest. I will say this shot hurts. I've talked to people and they're like, man, it really hurts going in. Yeah, I thought that was interesting.
- [59:05]
A
Yeah.
- [59:05]
C
Fair.
- [59:06]
A
Fair. All right, well, that's. That's it for this, this week's episode. I want to thank our listeners for joining us. I hope you learned a few things. I hope you laughed once or twice. Mostly. We're hoping you're planning to join us next week. And until then, I'm Matt Zyrus.
- [59:22]
C
I'm Tim Patton.
- [59:23]
B
And I'm Laura Faris. And we are Derms.